Decreased Expression of TRPV4 Channels in HEI-OC1 Cells Induced by High Glucose Is Associated with Hearing Impairment.
10.3349/ymj.2018.59.9.1131
- Author:
Ying XING
1
;
Jie MING
;
Tao LIU
;
Nana ZHANG
;
Dingjun ZHA
;
Ying LIN
Author Information
1. Department of Endocrinology and Metabolism Disease, Xijing Hospital, Forth Military Medical University, Xi'an, China.
- Publication Type:Original Article
- Keywords:
TRPV4;
high glucose;
hearing impairment;
HEI-OC1 cells
- MeSH:
Apoptosis;
Blotting, Western;
Cell Death;
Cell Proliferation;
Enzyme-Linked Immunosorbent Assay;
Glucose*;
Hearing Loss*;
Hearing*;
Ion Channels;
Protein Kinases;
RNA, Messenger
- From:Yonsei Medical Journal
2018;59(9):1131-1137
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Previous reports have shown that hyperglycemia-induced inhibition of transient receptor potential vanilloid sub type 4 (TRPV4), a transient receptor potential ion channel, affects the severity of hearing impairment (HI). In this study, we explored the role of TRPV4 in HI using HEI-OC1 cells exposed to high glucose (HG). MATERIALS AND METHODS: HEI-OC1 cells were cultured in a HG environment (25 mM D-glucose) for 48 hours, and qRT-PCR and Western blotting were used to analyze the expression of TRPV4 at the mRNA and protein level. TRPV4 agonist (GSK1016790A) or antagonist (HC-067047) in cultured HEI-OC1 cells was used to obtain abnormal TRPV4 expression. Functional TRPV4 activity was assessed in cultured HEI-OC1 cells using the MTT assay and a cell death detection ELISA. RESULTS: TRPV4 agonists exerted protective effects against HG-induced HI, as evidenced by increased MTT levels and inhibition of apoptosis in HEI-OC1 cells. TRPV4 overexpression significantly increased protein levels of phosphorylated p38 mitogen-activated protein kinase (p-p38 MAPK), while TRPV4 antagonists had the opposite effect. Our results indicated that TRPV4 is a hyperglycemia-related factor that can inhibit cell proliferation and promote cell apoptosis by activating the MAPK signaling pathway in HEI-OC1 cells. CONCLUSION: Our results show that the overexpression of TRPV4 can attenuate cell death in HEI-OC1 cells exposed to HG.
